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One of the most important services provided by clinical cardiologists is monitoring the echocardiography-derived left ventricular ejection fraction (LVEF) in patients with a recent acute myocardial infarction (MI), with the intention of recommending an implantable cardioverter-defibrillator (ICD) for those with persistently low LVEF (≤35%). Consequently, the report of Brooks et al. (1) on positive and negative independent predictors of LVEF recovery at 90 days following an MI has great utility. The authors observed that the intuitive variables of LVEF at presentation, length of stay, prior MI, lateral wall motion abnormality at presentation, and peak troponin performed best in predicting recovery of LVEF to >35%; for recovery of LVEF to ≥50%, the predictors were the intuitive variables of LVEF at presentation, peak troponin, prior MI, and the counterintuitive variable of presentation with ventricular fibrillation (VF) or cardiac arrest (CA) (1). The accompanying Editorial by Lindsay dealt comprehensively with the vagaries befalling on the clinical cardiologists to monitor the recovery of post-MI LVEF and designating them in the title of his piece, “accountable to determine the need for ICD therapy” (2). But what is the mechanism of the counterintuitive finding of the superior improvement in the LVEF in the survivors of VF/CA, despite their association with higher troponin levels and low LVEF? The editorialist is probably on target by attributing the initial low LVEF, partially due to myocardial stunning (2), with a potential for rapid recovery. Indeed, it is conceivable that had the PREDICTS (PREDiction of ICd Treatment Study) study database (1) included a repeat echocardiography, for the survivors of VF/CA, 1 to 2 days after the initial assessment, the LVEF metric would not be different in the authors’ >35% and ≥50% improvement predictive models.

One can only speculate as to the mechanism(s) of the early reduced LVEF in the survivors of VF/CA. Perhaps the patients are in a Takotsubo syndrome (TTS)–like state, mediated by a heightened autonomic sympathetic nervous system activity (expected in VF/CA) and/or the associated epinephrine use (sometimes in excessive amounts), during resuscitation. Perhaps there are pathophysiology commonalities in the patients with TTS in general, epinephrine-triggered TTS (3), survivors of VF/CA with or without use of epinephrine during resuscitation (4), and in the hearts of prospective organ donors (5). The take-home message is that we should not rely on the immediate post-resuscitation LVEF to predict whether a post-MI survivor of VF/CA is a suitable candidate for an ICD implantation.

Footnotes

Please note: Dr. Madias has reported that he has no relationships relevant to the contents of this paper to disclose.

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